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OBG · Gynaecological endocrinology: route of oestrogen in HRT
Sample itemWhy is transdermal oestradiol associated with a lower risk of venous thromboembolism than oral oestrogen in menopausal hormone therapy?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
C. It avoids first-pass hepatic metabolism, so clotting factor synthesis is not raised
Oral oestrogen passes through the liver first and increases synthesis of clotting factors, which raises thrombotic risk. Transdermal oestradiol enters the circulation directly and has little hepatic effect. A woman with a uterus still needs a progestogen with any oestrogen to protect the endometrium.
Option by option
A. It does not stimulate the endometrium, so no progestogen is needed
The endometrium is still stimulated, and a progestogen is needed if the uterus is present.
B. It is converted to oestriol, which is not thrombogenic
Transdermal oestradiol is not converted to oestriol in a way that explains the lower risk.
C. It avoids first-pass hepatic metabolism, so clotting factor synthesis is not raised (correct)
Correct. Bypassing the liver avoids the rise in clotting factors.
D. It blocks oestrogen receptors in the liver
Oestradiol is an agonist and does not block hepatic receptors.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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